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[PMID]:28648460
[Au] Autor:Huang CY; Ahmed AF; Su JH; Sung PJ; Hwang TL; Chiang PL; Dai CF; Liaw CC; Sheu JH
[Ad] Endereço:Department of Marine Biotechnology and Resources, National Sun Yat-sen University, Kaohsiung 804, Taiwan.
[Ti] Título:Bioactive new withanolides from the cultured soft coral Sinularia brassica.
[So] Source:Bioorg Med Chem Lett;27(15):3267-3271, 2017 08 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Continuing study of the ethyl acetate (EtOAc) extract of the cultured soft coral Sinularia brassica afforded five new withanolides, sinubrasolides H-L (1-5). The structures of the new compounds were elucidated on the basis of spectroscopic analysis. The cytotoxicities of new compounds 1-5 and a known compound sinubrasolide A (6) against the proliferation of a limited panel of cancer cell lines were assayed. The anti-inflammatory activities of compounds 1-6 were evaluated by measuring their ability to suppress N-formyl-methionyl-leucyl-phenyl-alanine/cytochalasin B (fMLP/CB)-induced superoxide anion generation and elastase release in human neutrophils.
[Mh] Termos MeSH primário: Antozoários/química
Anti-Inflamatórios/química
Anti-Inflamatórios/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Vitanolídeos/química
Vitanolídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/isolamento & purificação
Antineoplásicos/isolamento & purificação
Linhagem Celular Tumoral
Citocalasina B/imunologia
Seres Humanos
Modelos Moleculares
Neoplasias/tratamento farmacológico
Neutrófilos/efeitos dos fármacos
Elastase Pancreática/imunologia
Superóxidos/imunologia
Vitanolídeos/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antineoplastic Agents); 0 (Withanolides); 11062-77-4 (Superoxides); 3CHI920QS7 (Cytochalasin B); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE


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[PMID]:28322926
[Au] Autor:Gunnink LK; Busscher BM; Wodarek JA; Rosette KA; Strohbehn LE; Looyenga BD; Louters LL
[Ad] Endereço:Department of Chemistry and Biochemistry, Calvin College, Grand Rapids, MI 49546, USA.
[Ti] Título:Caffeine inhibition of GLUT1 is dependent on the activation state of the transporter.
[So] Source:Biochimie;137:99-105, 2017 Jun.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Caffeine has been shown to be a robust uncompetitive inhibitor of glucose uptake in erythrocytes. It preferentially binds to the nucleotide-binding site on GLUT1 in its tetrameric form and mimics the inhibitory action of ATP. Here we demonstrate that caffeine is also a dose-dependent, uncompetitive inhibitor of 2-deoxyglucose (2DG) uptake in L929 fibroblasts. The inhibitory effect on 2DG uptake in these cells was reversible with a rapid onset and was additive to the competitive inhibitory effects of glucose itself, confirming that caffeine does not interfere with glucose binding. We also report for the first time that caffeine inhibition was additive to inhibition by curcumin, suggesting distinct binding sites for curcumin and caffeine. In contrast, caffeine inhibition was not additive to that of cytochalasin B, consistent with previous data that reported that these two inhibitors have overlapping binding sites. More importantly, we show that the magnitude of maximal caffeine inhibition in L929 cells is much lower than in erythrocytes (35% compared to 90%). Two epithelial cell lines, HCLE and HK2, have both higher concentrations of GLUT1 and increased basal 2DG uptake (3-4 fold) compared to L929 cells, and subsequently display greater maximal inhibition by caffeine (66-70%). Interestingly, activation of 2DG uptake (3-fold) in L929 cells by glucose deprivation shifted the responsiveness of these cells to caffeine inhibition (35%-70%) without a change in total GLUT1 concentration. These data indicate that the inhibition of caffeine is dependent on the activity state of GLUT1, not merely on the concentration.
[Mh] Termos MeSH primário: Cafeína/farmacologia
Desoxiglucose/metabolismo
Células Epiteliais/efeitos dos fármacos
Eritrócitos/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Transportador de Glucose Tipo 1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Transporte Biológico
Western Blotting
Estimulantes do Sistema Nervoso Central/farmacologia
Citocalasina B/farmacologia
Células Epiteliais/metabolismo
Eritrócitos/metabolismo
Fibroblastos/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (Glucose Transporter Type 1); 0 (SLC2A1 protein, human); 3CHI920QS7 (Cytochalasin B); 3G6A5W338E (Caffeine); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28279980
[Au] Autor:McMillin SL; Schmidt DL; Kahn BB; Witczak CA
[Ad] Endereço:Department of Kinesiology, East Carolina University, Greenville, NC.
[Ti] Título:GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle.
[So] Source:Diabetes;66(6):1491-1500, 2017 Jun.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [ H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [ H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake.
[Mh] Termos MeSH primário: Transportador de Glucose Tipo 4/genética
Glucose/metabolismo
Músculo Esquelético/metabolismo
Suporte de Carga
[Mh] Termos MeSH secundário: Animais
Citocalasina B/farmacologia
Desoxiglucose/metabolismo
Frutose/farmacologia
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Transportador de Glucose Tipo 1/metabolismo
Transportador de Glucose Tipo 2
Transportador de Glucose Tipo 4/metabolismo
Hipertrofia/genética
Immunoblotting
Camundongos
Camundongos Knockout
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/patologia
Florizina/farmacologia
Trítio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transport Proteins, Facilitative); 0 (Glucose Transporter Type 1); 0 (Glucose Transporter Type 2); 0 (Glucose Transporter Type 4); 0 (Slc2A10 protein, mouse); 0 (Slc2a1 protein, mouse); 0 (Slc2a12 protein, mouse); 0 (Slc2a2 protein, mouse); 0 (Slc2a4 protein, mouse); 0 (Slc2a5 protein, mouse); 0 (Slc2a8 protein, mouse); 0 (Slc2a9 protein, mouse); 10028-17-8 (Tritium); 30237-26-4 (Fructose); 3CHI920QS7 (Cytochalasin B); 9G2MP84A8W (Deoxyglucose); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1075


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[PMID]:27965450
[Au] Autor:Cushion MT; Collins MS; Sesterhenn T; Porollo A; Vadukoot AK; Merino EJ
[Ad] Endereço:University of Cincinnati College of Medicine, Cincinnati, Ohio, USA Melanie.cushion@uc.edu.
[Ti] Título:Functional Characterization of Pneumocystis carinii Inositol Transporter 1.
[So] Source:MBio;7(6), 2016 Dec 13.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fungi in the genus Pneumocystis live in the lungs of mammals, where they can cause a fatal pneumonia (PCP [Pneumocystis pneumonia]) in hosts with compromised immune systems. The absence of a continuous in vitro culture system for any species of Pneumocystis has led to limited understanding of these fungi, especially for the discovery of new therapies. We recently reported that Pneumocystis carinii, Pneumocystis murina, and most significantly, Pneumocystis jirovecii lack both enzymes necessary for myo-inositol biosynthesis but contain genes with homologies to fungal myo-inositol transporters. Since myo-inositol is essential for eukaryotic viability, the primary transporter, ITR1, was functionally and structurally characterized in P. carinii The predicted structure of P. carinii ITR1 (PcITR1) contained 12 transmembrane alpha-helices with intracellular C and N termini, consistent with other inositol transporters. The apparent K was 0.94 ± 0.08 (mean ± standard deviation), suggesting that myo-inositol transport in P. carinii is likely through a low-affinity, highly selective transport system, as no other sugars or inositol stereoisomers were significant competitive inhibitors. Glucose transport was shown to use a different transport system. The myo-inositol transport was distinct from mammalian transporters, as it was not sodium dependent and was cytochalasin B resistant. Inositol transport in these fungi offers an attractive new drug target because of the reliance of the fungi on its transport, clear differences between the mammalian and fungal transporters, and the ability of the host to both synthesize and transport this critical nutrient, predicting low toxicity of potential inhibitors to the fungal transporter. IMPORTANCE: myo-Inositol is a sugarlike nutrient that is essential for life in most organisms. Humans and microbes alike can obtain it by making it, which involves only 2 enzymes, by taking it from the environment by a transport process, or by recycling it from other cellular constituents. Inspection of the genomes of the pathogenic fungi of the genus Pneumocystis showed that these pneumonia-causing parasites could not make myo-inositol, as they lacked the 2 enzymes. Instead, we found evidence of inositol transporters, which would import the sugar from the lungs where the fungi reside. In the present report, we characterized the transport of myo-inositol in the fungus and found that the transporter was highly selective for myo-inositol and did not transport any other molecules. The transport was distinct from that in mammalian cells, and since mammals can both make and transport myo-inositol, while Pneumocystis fungi must transport it, this process offers a potential new drug target.
[Mh] Termos MeSH primário: Proteínas Fúngicas/química
Proteínas Fúngicas/metabolismo
Inositol/metabolismo
Proteínas de Membrana Transportadoras/química
Proteínas de Membrana Transportadoras/metabolismo
Pneumocystis carinii/genética
[Mh] Termos MeSH secundário: Transporte Biológico
Metabolismo dos Carboidratos
Citocalasina B/metabolismo
Proteínas Fúngicas/genética
Glucose/metabolismo
Inositol/química
Cinética
Proteínas de Membrana Transportadoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Membrane Transport Proteins); 3CHI920QS7 (Cytochalasin B); 4L6452S749 (Inositol); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE


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[PMID]:27836974
[Au] Autor:Ojelabi OA; Lloyd KP; Simon AH; De Zutter JK; Carruthers A
[Ad] Endereço:From the Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01605.
[Ti] Título:WZB117 (2-Fluoro-6-(m-hydroxybenzoyloxy) Phenyl m-Hydroxybenzoate) Inhibits GLUT1-mediated Sugar Transport by Binding Reversibly at the Exofacial Sugar Binding Site.
[So] Source:J Biol Chem;291(52):26762-26772, 2016 Dec 23.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:WZB117 (2-fluoro-6-(m-hydroxybenzoyloxy) phenyl m-hydroxybenzoate) inhibits passive sugar transport in human erythrocytes and cancer cell lines and, by limiting glycolysis, inhibits tumor growth in mice. This study explores how WZB117 inhibits the erythrocyte sugar transporter glucose transport protein 1 (GLUT1) and examines the transporter isoform specificity of inhibition. WZB117 reversibly and competitively inhibits erythrocyte 3-O-methylglucose (3MG) uptake with K = 6 µm but is a noncompetitive inhibitor of sugar exit. Cytochalasin B (CB) is a reversible, noncompetitive inhibitor of 3MG uptake with K = 0.3 µm but is a competitive inhibitor of sugar exit indicating that WZB117 and CB bind at exofacial and endofacial sugar binding sites, respectively. WZB117 inhibition of GLUTs expressed in HEK293 cells follows the order of potency: insulin-regulated GLUT4 ≫ GLUT1 ≈ neuronal GLUT3. This may explain WZB117-induced murine lipodystrophy. Molecular docking suggests the following. 1) The WZB117 binding envelopes of exofacial GLUT1 and GLUT4 conformers differ significantly. 2) GLUT1 and GLUT4 exofacial conformers present multiple, adjacent glucose binding sites that overlap with WZB117 binding envelopes. 3) The GLUT1 exofacial conformer lacks a CB binding site. 4) The inward GLUT1 conformer presents overlapping endofacial WZB117, d-glucose, and CB binding envelopes. Interrogating the GLUT1 mechanism using WZB117 reveals that subsaturating WZB117 and CB stimulate erythrocyte 3MG uptake. Extracellular WZB117 does not affect CB binding to GLUT1, but intracellular WZB117 inhibits CB binding. These findings are incompatible with the alternating conformer carrier for glucose transport but are consistent with either a multisubunit, allosteric transporter, or a transporter in which each subunit presents multiple, interacting ligand binding sites.
[Mh] Termos MeSH primário: 3-O-Metilglucose/metabolismo
Eritrócitos/metabolismo
Transportador de Glucose Tipo 1/metabolismo
Glucose/metabolismo
Hidroxibenzoatos/farmacologia
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Transporte Biológico
Cristalografia por Raios X
Citocalasina B/metabolismo
Eritrócitos/efeitos dos fármacos
Transportador de Glucose Tipo 1/química
Transportador de Glucose Tipo 3/química
Transportador de Glucose Tipo 3/metabolismo
Transportador de Glucose Tipo 4/química
Transportador de Glucose Tipo 4/metabolismo
Células HEK293
Seres Humanos
Cinética
Camundongos
Simulação de Acoplamento Molecular
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 1); 0 (Glucose Transporter Type 3); 0 (Glucose Transporter Type 4); 0 (Hydroxybenzoates); 0 (SLC2A1 protein, human); 0 (SLC2A3 protein, human); 0 (SLC2A4 protein, human); 0 (WZB117); 146-72-5 (3-O-Methylglucose); 3CHI920QS7 (Cytochalasin B); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161113
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.759175


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[PMID]:27640744
[Au] Autor:Chang HT; Chou CT; Chen IS; Yu CC; Lu T; Hsu SS; Shieh P; Jan CR; Liang WZ
[Ad] Endereço:Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan, ROC.
[Ti] Título:Mechanisms underlying effect of the mycotoxin cytochalasin B on induction of cytotoxicity, modulation of cell cycle, Ca homeostasis and ROS production in human breast cells.
[So] Source:Toxicology;370:1-19, 2016 Aug 31.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Cytochalasin B, a cell-permeable mycotoxin isolated from the fungus Phoma spp., shows a wide range of biological effects, among which its potent antitumor activity has raised great interests in different models. However, the cytotoxic activity of cytochalasin B and its underlying mechanisms have not been elucidated in breast cells. This study examined the effect of cytochalasin B on MCF 10A human breast epithelial cells and ZR-75-1 human breast cancer cells. Cytochalasin B (10-20µM) concentration-dependently induced cytotoxicity, cell cycle arrest, and [Ca ] rises in ZR-75-1 cells but not in MCF 10A cells. In ZR-75-1 cells, cytochalasin B triggered G2/M phase arrest through the modulation of CDK1, cyclin B1, p53, p27 and p21 expressions. The Ca signal response induced by cytochalasin B was reduced by removing extracellular Ca and was inhibited by the store-operated Ca channel blocker 2-APB and SKF96365. In Ca -free medium, cytochalasin B induced Ca release through thapsigargin-sensitive endoplasmic reticulum stores. Moreover, cytochalasin B increased H O levels but reduced GSH levels. The apoptotic effects evoked by cytochalasin B were partially inhibited by prechelating cytosolic Ca with BAPTA-AM and the antioxidant NAC. Together, in ZR-75-1 cells but not in MCF 10A cells, cytochalasin B activated Ca -associated mitochondrial apoptotic pathways that involved G2/M phase arrest and ROS signaling. Furthermore, cytochalasin B induced [Ca ] rises by releasing Ca from the endoplasmic reticulum and causing Ca influx through 2-APB or SKF96365-sensitive store-operated Ca entry. Our findings provide new insights into the possible application of cytochalasin B in human breast cancer therapy.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Ciclo Celular/efeitos dos fármacos
Citocalasina B/farmacologia
Células Epiteliais/efeitos dos fármacos
Homeostase/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Mama/citologia
Neoplasias da Mama/tratamento farmacológico
Proteína Quinase CDC2
Sinalização do Cálcio/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Ciclina B1/genética
Ciclina B1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Quinases Ciclina-Dependentes/genética
Quinases Ciclina-Dependentes/metabolismo
Retículo Endoplasmático/efeitos dos fármacos
Células Epiteliais/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNB1 protein, human); 0 (CDKN1A protein, human); 0 (CDKN1B protein, human); 0 (Cyclin B1); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Reactive Oxygen Species); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); 3CHI920QS7 (Cytochalasin B); BBX060AN9V (Hydrogen Peroxide); EC 2.7.11.22 (CDC2 Protein Kinase); EC 2.7.11.22 (CDK1 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160920
[St] Status:MEDLINE


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[PMID]:27581081
[Au] Autor:Hou X; Liu J; Zhang Z; Zhai Y; Wang Y; Wang Z; Tang B; Zhang X; Sun L; Li Z
[Ad] Endereço:State and Local Joint Engineering Laboratory for Animal Models of Human DiseasesAcademy of Translational Medicine, First Hospital, Jilin University, Changchun, Jilin, China College of Animal ScienceJilin University, Changchun, Jilin, China.
[Ti] Título:Effects of cytochalasin B on DNA methylation and histone modification in parthenogenetically activated porcine embryos.
[So] Source:Reproduction;152(5):519-27, 2016 Nov.
[Is] ISSN:1741-7899
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:DNA methylation and histone modification play important roles in the development of mammalian embryos. Cytochalasin B (CB) is an actin polymerization inhibitor that can significantly affect cell activity and is often used in studies concerning cytology. In recent years, CB is also commonly being used in in vitro experiments on mammalian embryos, but few studies have addressed the effect of CB on the epigenetic modification of embryonic development, and the mechanism underlying this process is also unknown. This study was conducted to investigate the effects of CB on DNA methylation and histone modification in the development of parthenogenetically activated porcine embryos. Treatment with 5 µg/mL CB for 4 h significantly increased the cleavage rate, blastocyst rate and total cell number of blastocysts. However, the percentage of apoptotic cells and the expression levels of the apoptosis-related genes BCL-XL, BAX and CASP3 were significantly decreased. Treatment with CB significantly decreased the expression levels of DNMT1, DNMT3a, DNMT3b, HAT1 and HDAC1 at the pronuclear stage and promoted the conversion of 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC). After CB treatment, the level of AcH3K9 was upregulated and the level of H3K9me3 was downregulated. When combined with Scriptaid and 5-Aza-Cdr, CB further improved the embryonic development competence and decreased the expression of BCL-XL, BAX and CASP3 In conclusion, these results suggest that CB could improve embryonic development and the quality of the blastocyst by improving the epigenetic modification during the development of parthenogenetically activated embryos.
[Mh] Termos MeSH primário: Blastocisto/citologia
Citocalasina B/farmacologia
Metilação de DNA/efeitos dos fármacos
Embrião de Mamíferos/citologia
Desenvolvimento Embrionário/efeitos dos fármacos
Histonas/química
Partenogênese
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Blastocisto/efeitos dos fármacos
Blastocisto/metabolismo
DNA (Citosina-5-)-Metiltransferases/metabolismo
Embrião de Mamíferos/efeitos dos fármacos
Embrião de Mamíferos/metabolismo
Epigênese Genética
Feminino
Inibidores de Histona Desacetilases/farmacologia
Histonas/metabolismo
Técnicas de Transferência Nuclear
Gravidez
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histone Deacetylase Inhibitors); 0 (Histones); 3CHI920QS7 (Cytochalasin B); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNA methyltransferase 3B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE
[do] DOI:10.1530/REP-16-0280


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[PMID]:27567521
[Au] Autor:Feitosa AO; Dias AC; Ramos GD; Bitencourt HR; Siqueira JE; Marinho PS; Barison A; Ocampos FM; Marinho AM
[Ad] Endereço:Universidade Federal do Pará, Instituto de Ciências Exatas e Naturais-Programa de Pós-graduação em Química, Belém, Pará, Brazil.
[Ti] Título:Lethality of cytochalasin B and other compounds isolated from fungus Aspergillus sp. (Trichocomaceae) endophyte of Bauhinia guianensis (Fabaceae).
[So] Source:Rev Argent Microbiol;48(3):259-263, 2016 Jul - Sep.
[Is] ISSN:0325-7541
[Cp] País de publicação:Argentina
[La] Idioma:eng
[Ab] Resumo:Endophytic fungi are fungi that colonize internal tissues of plants; several biologically active compounds have been isolated from these fungi. There are few studies of compounds isolated from endophytic fungi of Amazon plants. Thus, this study aimed the isolation and structural identification of ergosterol (1), ergosterol peroxide (2), mevalonolactone (3), cytochalasin B (4) and cytochalasin H (5) from Aspergillus sp. EJC 04, an endophytic fungus from Bauhinia guianensis. The cytochalasin B (4) and the diacetate derivative of cytochalasin B (4a) showed high lethality in the brine shrimp assay. This is the first occurrence of cytochalasins in Amazonian endophytic fungi from B. guianensis.
[Mh] Termos MeSH primário: Artemia/efeitos dos fármacos
Aspergillus/química
Citocalasina B/toxicidade
Citocalasinas/toxicidade
Endófitos/química
Ergosterol/análogos & derivados
Fabaceae/microbiologia
Ácido Mevalônico/análogos & derivados
[Mh] Termos MeSH secundário: Acetilação
Animais
Argentina
Aspergillus/isolamento & purificação
Citocalasina B/química
Citocalasina B/isolamento & purificação
Citocalasinas/química
Citocalasinas/isolamento & purificação
Endófitos/isolamento & purificação
Ergosterol/química
Ergosterol/isolamento & purificação
Ergosterol/toxicidade
Dose Letal Mediana
Ácido Mevalônico/química
Ácido Mevalônico/isolamento & purificação
Ácido Mevalônico/toxicidade
Estrutura Molecular
Ressonância Magnética Nuclear Biomolecular
Espectrometria de Massas por Ionização por Electrospray
Relação Estrutura-Atividade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochalasins); 3CHI920QS7 (Cytochalasin B); 53760-19-3 (cytochalasin H); 661X270Z3L (mevalonolactone); S5UOB36OCZ (Mevalonic Acid); UG9TN81TGH (ergosterol-5,8-peroxide); Z30RAY509F (Ergosterol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160829
[St] Status:MEDLINE


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[PMID]:27401755
[Au] Autor:Clow KA; Short CE; Hall JR; Gendron RL; Paradis H; Ralhan A; Driedzic WR
[Ad] Endereço:Department of Ocean Sciences, Ocean Sciences Centre, Memorial University of Newfoundland, St John's, NL, Canada A1C 5S7.
[Ti] Título:High rates of glucose utilization in the gas gland of Atlantic cod (Gadus morhua) are supported by GLUT1 and HK1b.
[So] Source:J Exp Biol;219(Pt 17):2763-73, 2016 Sep 01.
[Is] ISSN:1477-9145
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The gas gland of physoclistous fish utilizes glucose to generate lactic acid that leads to the off-loading of oxygen from haemoglobin. This study addresses characteristics of the first two steps in glucose utilization in the gas gland of Atlantic cod (Gadus morhua). Glucose metabolism by isolated gas gland cells was 12- and 170-fold higher, respectively, than that in heart and red blood cells (RBCs) as determined by the production of (3)H2O from [2-(3)H]glucose. In the gas gland, essentially all of the glucose consumed was converted to lactate. Glucose uptake in the gas gland shows a very high dependence upon facilitated transport as evidenced by saturation of uptake of 2-deoxyglucose at a low extracellular concentration and a requirement for high levels of cytochalasin B for uptake inhibition despite the high efficacy of this treatment in heart and RBCs. Glucose transport is via glucose transporter 1 (GLUT1), which is localized to the glandular cells. GLUT1 western blot analysis from whole-tissue lysates displayed a band with a relative molecular mass of 52 kDa, consistent with the deduced amino acid sequence. Levels of 52 kDa GLUT1 in the gas gland were 2.3- and 33-fold higher, respectively, than those in heart and RBCs, respectively. Glucose phosphorylation is catalysed by hexokinase Ib (HKIb), a paralogue that cannot bind to the outer mitochondrial membrane. Transcript levels of HKIb in the gas gland were 52- and 57-fold more abundant, respectively, than those in heart and RBCs. It appears that high levels of GLUT1 protein and an unusual isoform of HKI are both critical for the high rates of glycolysis in gas gland cells.
[Mh] Termos MeSH primário: Estruturas Animais/metabolismo
Gadus morhua/anatomia & histologia
Gadus morhua/metabolismo
Gases/metabolismo
Transportador de Glucose Tipo 1/metabolismo
Glucose/metabolismo
Hexoquinase/metabolismo
[Mh] Termos MeSH secundário: Estruturas Animais/citologia
Animais
Separação Celular
Citocalasina B/farmacologia
Desoxiglucose/metabolismo
Eritrócitos/metabolismo
Imuno-Histoquímica
Ácido Láctico/metabolismo
Peso Molecular
Transporte Proteico/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gases); 0 (Glucose Transporter Type 1); 0 (RNA, Messenger); 33X04XA5AT (Lactic Acid); 3CHI920QS7 (Cytochalasin B); 9G2MP84A8W (Deoxyglucose); EC 2.7.1.1 (Hexokinase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1242/jeb.141721


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[PMID]:27368805
[Au] Autor:Kustiawan I; Derksen N; Rispens T
[Ad] Endereço:Sanquin Research, Department of Immunopathology, Amsterdam, The Netherlands; Landsteiner Laboratory, Academic Medical Centre, University of Amsterdam, The Netherlands.
[Ti] Título:Inactivated pepsin inhibits neutrophil activation by Fcgamma-receptor-dependent and independent stimuli.
[So] Source:Clin Immunol;169:85-88, 2016 Aug.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pepsin is widely used to produce F(ab')2 fragments of immunoglobulin G (IgG). In many cases, at least part of the pepsin will remain present in the F(ab')2 preparation, albeit in (irreversibly) inactivated form. Here we report on a potent immunomodulatory effect of irreversibly inactivated pepsin on activated human neutrophils. Degranulation, induced by coated IgG or via cytochalasin B/N-formyl-Met-Leu-Phe, was measured by quantifying elastase release, and was found to be inhibited in a dose-dependent manner by inactivated pepsin. Since a number of intravenous immunoglobulin (IVIg) products are also treated by limited digestion with pepsin, we investigated if pepsin would be present in quantities large enough to inhibit neutrophil activation. The amounts of pepsin detected in three different pepsin-treated IVIg products were found to be too low to induce an effect, at least in an in vitro setting.
[Mh] Termos MeSH primário: Fragmentos Fab das Imunoglobulinas/farmacologia
Ativação de Neutrófilo/efeitos dos fármacos
Neutrófilos/efeitos dos fármacos
Pepsina A/farmacologia
Receptores de IgG/metabolismo
[Mh] Termos MeSH secundário: Degranulação Celular/efeitos dos fármacos
Células Cultivadas
Citocalasina B/farmacologia
Relação Dose-Resposta a Droga
Ativação Enzimática
Seres Humanos
Fragmentos Fab das Imunoglobulinas/metabolismo
Imunoglobulina G/metabolismo
Imunoglobulina G/farmacologia
Imunoglobulinas Intravenosas/metabolismo
Imunoglobulinas Intravenosas/farmacologia
Elastase de Leucócito/metabolismo
Masculino
N-Formilmetionina Leucil-Fenilalanina/farmacologia
Neutrófilos/metabolismo
Pepsina A/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FCGR1A protein, human); 0 (Immunoglobulin Fab Fragments); 0 (Immunoglobulin G); 0 (Immunoglobulins, Intravenous); 0 (Receptors, IgG); 3CHI920QS7 (Cytochalasin B); 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine); EC 3.4.21.37 (Leukocyte Elastase); EC 3.4.23.1 (Pepsin A)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170813
[Lr] Data última revisão:
170813
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160703
[St] Status:MEDLINE



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